DHEA Increases Foam Cell Formation
NEW YORK (Reuters Health) Dec 05 - Dehydroepiandrosterone (DHEA), a supplement popular with men for its possible anti-aging effects, seems to increase macrophage foam cell formation in vitro, Australian researchers report. This means it could raise the risk of atherosclerotic disease.
In the U.S., DHEA is available without a prescription and, in recent years, there has been a rapid rise in unsupervised use of the drug. Despite DHEA's popularity, its effects on vascular biology are largely unknown, according to Dr. David S. Celermajer, from the Royal Prince Alfred Hospital in Sydney, and colleagues.
As described in the December 3rd issue of the Journal of the American College of Cardiology, the researchers conducted several in vitro experiments to determine how DHEA affects monocyte adhesion to vascular endothelium and human foam cell formation.
DHEA promoted foam cell formation, the authors note. Treatment with the agent caused a dose-dependent rise in male macrophage cholesterol ester content. This effect seemed to be mediated by the androgen receptor and involved an upregulation of two key lipoprotein-processing enzymes.
In contrast, DHEA did not have a significant effect on monocyte-endothelial adhesion or on endothelial cell expression of cell adhesion molecules, the investigators report.
"The potentially pro-atherogenic effect of DHEA on male macrophage foam cell formation is consistent with available interpopulation and age-specific epidemiologic data on DHEA concentrations, in the context of the natural history of atherosclerosis," Dr. Celermajer's team notes.
"Further basic and clinical studies are required to further elucidate the potentially adverse cardiovascular effects of DHEA," they add.
J Am Coll Cardiol 2003;42:1967-1974.
NEW YORK (Reuters Health) Dec 05 - Dehydroepiandrosterone (DHEA), a supplement popular with men for its possible anti-aging effects, seems to increase macrophage foam cell formation in vitro, Australian researchers report. This means it could raise the risk of atherosclerotic disease.
In the U.S., DHEA is available without a prescription and, in recent years, there has been a rapid rise in unsupervised use of the drug. Despite DHEA's popularity, its effects on vascular biology are largely unknown, according to Dr. David S. Celermajer, from the Royal Prince Alfred Hospital in Sydney, and colleagues.
As described in the December 3rd issue of the Journal of the American College of Cardiology, the researchers conducted several in vitro experiments to determine how DHEA affects monocyte adhesion to vascular endothelium and human foam cell formation.
DHEA promoted foam cell formation, the authors note. Treatment with the agent caused a dose-dependent rise in male macrophage cholesterol ester content. This effect seemed to be mediated by the androgen receptor and involved an upregulation of two key lipoprotein-processing enzymes.
In contrast, DHEA did not have a significant effect on monocyte-endothelial adhesion or on endothelial cell expression of cell adhesion molecules, the investigators report.
"The potentially pro-atherogenic effect of DHEA on male macrophage foam cell formation is consistent with available interpopulation and age-specific epidemiologic data on DHEA concentrations, in the context of the natural history of atherosclerosis," Dr. Celermajer's team notes.
"Further basic and clinical studies are required to further elucidate the potentially adverse cardiovascular effects of DHEA," they add.
J Am Coll Cardiol 2003;42:1967-1974.
